Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2001-1-26
pubmed:abstractText
Impaired NGF production and release has been documented in aged animals, suggesting that decreased NGF receptor stimulation may be one factor contributing to neuronal dysfunction with aging. Other studies have suggested that aging may be associated with impaired intracellular responses to NGF. Because aging-associated neuronal dysfunction contributes to morbidity and mortality in the geriatric population, it is important to determine whether the effects of aging on sensory neuron function and survival are reversible. In the present study, we observed significantly decreased neurite outgrowth and neuronal survival in short-term cultures (0-96 h) of dorsal root ganglion (DRG) neurons from aged (>22 months) Fisher 344 x Brown Norway F1 hybrid rats, compared to young (4-6 month) and middle-aged (14 month) animals. From 24 to 96 h in culture, diminished survival of aged neurons appeared to be due to an increased rate of apoptotic cell death. DRG neurons from aged animals also exhibited significantly decreased whole cell, high-threshold voltage-dependent calcium currents, with a larger proportion of L-type current, compared to youthful and middle-aged animals. Treatment of aged DRG neurons with NGF restored neurite outgrowth, neuronal survival and calcium current amplitude and subtype distribution to those observed in youthful DRG neurons.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
888
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
128-137
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11146059-Animals, pubmed-meshheading:11146059-Apoptosis, pubmed-meshheading:11146059-Calcium, pubmed-meshheading:11146059-Calcium Channels, L-Type, pubmed-meshheading:11146059-Calcium Signaling, pubmed-meshheading:11146059-Cell Aging, pubmed-meshheading:11146059-Cell Survival, pubmed-meshheading:11146059-Cells, Cultured, pubmed-meshheading:11146059-Culture Media, Serum-Free, pubmed-meshheading:11146059-Ganglia, Spinal, pubmed-meshheading:11146059-In Situ Nick-End Labeling, pubmed-meshheading:11146059-Male, pubmed-meshheading:11146059-Membrane Potentials, pubmed-meshheading:11146059-Nerve Growth Factor, pubmed-meshheading:11146059-Neurites, pubmed-meshheading:11146059-Neurons, Afferent, pubmed-meshheading:11146059-Patch-Clamp Techniques, pubmed-meshheading:11146059-Rats, pubmed-meshheading:11146059-Rats, Inbred BN, pubmed-meshheading:11146059-Rats, Inbred F344
pubmed:year
2001
pubmed:articleTitle
Treatment of aged rat sensory neurons in short-term, serum-free culture with nerve growth factor reverses the effect of aging on neurite outgrowth, calcium currents, and neuronal survival.
pubmed:affiliation
Department of Internal Medicine, Ann Arbor VA Medical Center, University of Michigan, GRECC 11G, D-318, Ann Arbor, MI 48105-2399, USA. kehall@umich.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, U.S. Gov't, Non-P.H.S., Research Support, Non-U.S. Gov't